title: Gastric emptying, incretin hormone secretion, and postprandial glycemia in cystic fibrosis--effects of pancreatic enzyme supplementation.
abstract: BACKGROUND
  Postprandial hyperglycemia is an important clinical problem in cystic fibrosis (CF), but the contribution of fat malabsorption, rapid gastric emptying, and the incretin axis has not been widely considered.
  
  
  OBJECTIVE
  The aim of this study was to evaluate these aspects of gut function in nondiabetic CF patients.
  
  
  METHODS
  We conducted a randomized, double-blind, placebo-controlled crossover study at a clinical research laboratory.
  
  
  METHODS
  Five nondiabetic CF patients (three males; age, 25.8 ± 1.0 yr; body mass index, 20.2 ± 1.1 kg/m(2)) with exocrine pancreatic insufficiency and six healthy subjects of similar age and body mass index participated in the study.
  
  
  METHODS
  CF patients consumed a radiolabeled mashed potato meal on 2 separate days, together with four capsules of Creon Forte (100,000 IU lipase) or placebo. Healthy subjects consumed the meal once, without pancreatic enzymes.
  
  
  METHODS
  Gastric emptying was measured using scintigraphy, and blood was sampled frequently for blood glucose and plasma glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and glucagon concentrations.
  
  
  RESULTS
  CF patients had more rapid gastric emptying (P < 0.001), impaired secretion of GLP-1 (P < 0.01) and GIP (P < 0.001), and greater postprandial glycemic excursions (P < 0.001) than healthy subjects. Pancreatic enzyme supplementation normalized gastric emptying and GLP-1 secretion and tended to increase glucagon (P = 0.08), but did not completely restore GIP secretion or normalize postprandial blood glucose. There was an excellent correlation between gastric emptying and blood glucose concentration at 60 min (R = 0.75; P = 0.01).
  
  
  CONCLUSIONS
  Pancreatic enzyme supplementation plays an important role in incretin secretion, gastric emptying, and postprandial hyperglycemia in CF.
authors.affiliation: Discipline of Medicine, University of Adelaide, Level 6, Eleanor Harrald Building, Royal Adelaide Hospital, Adelaide 5000, Australia.
authors.forename: Paul
authors.initials: P
authors.lastname: Kuo
authors.forename: Julie E
authors.initials: JE
authors.lastname: Stevens
authors.forename: Antonietta
authors.initials: A
authors.lastname: Russo
authors.forename: Anne
authors.initials: A
authors.lastname: Maddox
authors.forename: Judith M
authors.initials: JM
authors.lastname: Wishart
authors.forename: Karen L
authors.initials: KL
authors.lastname: Jones
authors.forename: Hugh
authors.initials: H
authors.lastname: Greville
authors.forename: David
authors.initials: D
authors.lastname: Hetzel
authors.forename: Ian
authors.initials: I
authors.lastname: Chapman
authors.forename: Michael
authors.initials: M
authors.lastname: Horowitz
authors.forename: Christopher K
authors.initials: CK
authors.lastname: Rayner
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D003550:Cystic Fibrosis / Q000097:blood / Q000503:physiopathology*; D004040:Dietary Carbohydrates / Q000494:pharmacology; D004041:Dietary Fats / Q000494:pharmacology; D004311:Double-Blind Method; D005260:Female; D005746:Gastric Emptying / Q000502:physiology*; D005749:Gastric Inhibitory Polypeptide / Q000097:blood; D005934:Glucagon / Q000097:blood; D052216:Glucagon-Like Peptide 1 / Q000097:blood; D006801:Humans; D006943:Hyperglycemia / Q000378:metabolism*; D054795:Incretins / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D008049:Lipase / Q000627:therapeutic use*; D008297:Male; D010179:Pancreas / Q000201:enzymology*; D055815:Young Adult
chemical_list: D001786:Blood Glucose; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D054795:Incretins; D007328:Insulin; D005749:Gastric Inhibitory Polypeptide; D052216:Glucagon-Like Peptide 1; D005934:Glucagon; D008049:Lipase